Early changes in hepatic energy metabolism and lipid content in recent-onset type 1 and 2 diabetes mellitus
Non-alcoholic fatty liver disease (NAFLD) is associated with abnormal mitochondrial capacity. While oxidative capacity can be increased in steatosis, hepatic ATP decreases in long-standing diabetes. However, longitudinal studies on diabetes-related NAFLD and its relationship to hepatic energy metabo...
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| creator | Kupriyanova, Yuliya Zaharia, Oana Patricia Bobrov, Pavel Karusheva, Yanislava Burkart, Volker Szendroedi, Julia Hwang, Jong-Hee Roden, Michael Roden, M. Al-Hasani, H. Burkart, V. Buyken, A.E. Geerling, G. Hwang, J.H. Herder, C. Icks, A. Jandeleit-Dahm, K. Kahl, S. Kotzka, J. Kuss, O. Lammert, E. Trenkamp, S. Rathmann, W. Szendroedi, J. Ziegler, D. |
| description | Non-alcoholic fatty liver disease (NAFLD) is associated with abnormal mitochondrial capacity. While oxidative capacity can be increased in steatosis, hepatic ATP decreases in long-standing diabetes. However, longitudinal studies on diabetes-related NAFLD and its relationship to hepatic energy metabolism are lacking.
This prospective study comprised volunteers with type 1 (T1DM, n = 30) and type 2 (T2DM, n = 37) diabetes. At diagnosis and 5 years later, we used 1H/31P magnetic resonance spectroscopy to measure hepatocellular lipid (HCL), γATP and inorganic phosphate (Pi) concentrations, and to assess adipose tissue volumes. Insulin sensitivity was assessed by hyperinsulinemic-euglycemic clamps.
At diagnosis, individuals with T2DM had higher HCL and adipose tissue volumes, but lower whole-body insulin sensitivity than those with T1DM, despite comparable glycemic control. NAFLD was present in 38% of individuals with T2DM and 7% with T1DM. After 5 years, visceral adipose tissue only increased in individuals with T2DM, while HCL almost doubled in this group (p |
| doi_str_mv | 10.1016/j.jhep.2020.11.030 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2466292630</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0168827820338174</els_id><sourcerecordid>2553567847</sourcerecordid><originalsourceid>FETCH-LOGICAL-c428t-92b51e6130842f2b95059dec67c48968b620e87e3228a7586d0208748e5587893</originalsourceid><addsrcrecordid>eNp9kcFq3DAQhkVJaTZpX6CHIsilF2-lsSTL0EsIaRMI9NKehSzPJnJt2ZXkwL59tdm0hxxyGjF8-hj-n5CPnG054-rLsB0ecNkCg7LgW1azN2TDFWMVU4KfkE2BdKWh0afkLKWBsYK04h05rWuQrRZyQ35f2zjuqXuw4R4T9YEWpc3eUQwY7_d0wmy7efRpojb0dPSL76mbQ8aQD3hEV17VHBJmmvcLUv4EAu297TAX6YTj6POa3pO3Ozsm_PA8z8mvb9c_r26qux_fb68u7yonQOeqhU5yVLxmWsAOulYy2fboVOOEbpXuFDDUDdYA2jZSq74EoBuhUUrd6LY-J5-P3iXOf1ZM2Uw-uXKEDTivyYBQClpQNSvoxQt0mNcYynUGpKylarRoCgVHysU5pYg7s0Q_2bg3nJlDFWYwhyrMoQrDuWFP6k_P6rWbsP__5V_2Bfh6BLBk8egxmuQ8Boe9L6Fm08_-Nf9finSX6A</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2553567847</pqid></control><display><type>article</type><title>Early changes in hepatic energy metabolism and lipid content in recent-onset type 1 and 2 diabetes mellitus</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><creator>Kupriyanova, Yuliya ; Zaharia, Oana Patricia ; Bobrov, Pavel ; Karusheva, Yanislava ; Burkart, Volker ; Szendroedi, Julia ; Hwang, Jong-Hee ; Roden, Michael ; Roden, M. ; Al-Hasani, H. ; Burkart, V. ; Buyken, A.E. ; Geerling, G. ; Hwang, J.H. ; Herder, C. ; Icks, A. ; Jandeleit-Dahm, K. ; Kahl, S. ; Kotzka, J. ; Kuss, O. ; Lammert, E. ; Trenkamp, S. ; Rathmann, W. ; Szendroedi, J. ; Ziegler, D.</creator><creatorcontrib>Kupriyanova, Yuliya ; Zaharia, Oana Patricia ; Bobrov, Pavel ; Karusheva, Yanislava ; Burkart, Volker ; Szendroedi, Julia ; Hwang, Jong-Hee ; Roden, Michael ; Roden, M. ; Al-Hasani, H. ; Burkart, V. ; Buyken, A.E. ; Geerling, G. ; Hwang, J.H. ; Herder, C. ; Icks, A. ; Jandeleit-Dahm, K. ; Kahl, S. ; Kotzka, J. ; Kuss, O. ; Lammert, E. ; Trenkamp, S. ; Rathmann, W. ; Szendroedi, J. ; Ziegler, D. ; the GDS group ; GDS group</creatorcontrib><description>Non-alcoholic fatty liver disease (NAFLD) is associated with abnormal mitochondrial capacity. While oxidative capacity can be increased in steatosis, hepatic ATP decreases in long-standing diabetes. However, longitudinal studies on diabetes-related NAFLD and its relationship to hepatic energy metabolism are lacking.
This prospective study comprised volunteers with type 1 (T1DM, n = 30) and type 2 (T2DM, n = 37) diabetes. At diagnosis and 5 years later, we used 1H/31P magnetic resonance spectroscopy to measure hepatocellular lipid (HCL), γATP and inorganic phosphate (Pi) concentrations, and to assess adipose tissue volumes. Insulin sensitivity was assessed by hyperinsulinemic-euglycemic clamps.
At diagnosis, individuals with T2DM had higher HCL and adipose tissue volumes, but lower whole-body insulin sensitivity than those with T1DM, despite comparable glycemic control. NAFLD was present in 38% of individuals with T2DM and 7% with T1DM. After 5 years, visceral adipose tissue only increased in individuals with T2DM, while HCL almost doubled in this group (p <0.001), resulting in a 70% prevalence of NAFLD (independent of diabetes treatment). Changes in HCL correlated with adipose tissue volume and insulin resistance (r = 0.50 and r = 0.44, both p <0.05). Pi decreased by 17% and 10% in individuals with T2DM and T1DM (p <0.05), respectively. In T1DM, HCL did not change, whereas γATP decreased by 10% and correlated negatively with glycated hemoglobin (r = -0.56, p <0.05).
The rapid increase in HCL during the early course of T2DM likely results from enlarging adipose tissue volume and insulin resistance in response to impaired hepatic mitochondrial adaptation. The decrease of phosphorus metabolites in T1DM may be due to pharmacological insulin supply.
Previous studies suggested that the impaired function of mitochondria, the power plants of cells, can promote fatty liver and type 2 diabetes mellitus. This study now shows that during the first 5 years of type 2 diabetes the increase in body fat content rapidly leads to a doubling of liver fat content, whereas the energy metabolism of the patients' livers progressively declines. These data suggest that fat tissue mass and liver mitochondria have an important role in the development of fatty liver disease in humans with diabetes.
NCT01055093
[Display omitted]
•Hepatic lipids increase 2-fold in the early course of type 2 diabetes.•Patients with type 1 diabetes do not develop steatosis in first 5 years after diagnosis.•Adipose tissue mass and insulin resistance drive the development of steatosis.•Phosphorus metabolites decline in type 1 diabetes due to low portal insulin supply.</description><identifier>ISSN: 0168-8278</identifier><identifier>EISSN: 1600-0641</identifier><identifier>DOI: 10.1016/j.jhep.2020.11.030</identifier><identifier>PMID: 33259845</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Adipose tissue ; Adipose Tissue - diagnostic imaging ; Adipose Tissue - metabolism ; Adipose Tissue - pathology ; body composition ; Body Composition - physiology ; Body fat ; Body Fat Distribution ; Diabetes ; Diabetes mellitus (insulin dependent) ; Diabetes mellitus (non-insulin dependent) ; Diabetes Mellitus, Type 1 - diagnosis ; Diabetes Mellitus, Type 1 - metabolism ; Diabetes Mellitus, Type 2 - diagnosis ; Diabetes Mellitus, Type 2 - metabolism ; Diagnosis ; Energy metabolism ; Energy Metabolism - physiology ; Fatty liver ; Female ; Glycated Hemoglobin A - analysis ; Hemoglobin ; hepatocellular lipid content ; Humans ; Insulin ; Insulin resistance ; Insulin Resistance - physiology ; Lipid metabolism ; Lipid Metabolism - physiology ; Liver - metabolism ; Liver - pathology ; Liver diseases ; Magnetic resonance spectroscopy ; Magnetic Resonance Spectroscopy - methods ; Male ; Metabolism ; Metabolites ; Middle Aged ; Mitochondria ; Mitochondria, Liver - physiology ; Non-alcoholic Fatty Liver Disease - diagnosis ; Non-alcoholic Fatty Liver Disease - metabolism ; Phosphorus ; phosphorus metabolites ; Plant cells ; Power plants ; Steatosis</subject><ispartof>Journal of hepatology, 2021-05, Vol.74 (5), p.1028-1037</ispartof><rights>2020 European Association for the Study of the Liver</rights><rights>Copyright © 2020 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.</rights><rights>Copyright Elsevier Science Ltd. May 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c428t-92b51e6130842f2b95059dec67c48968b620e87e3228a7586d0208748e5587893</citedby><cites>FETCH-LOGICAL-c428t-92b51e6130842f2b95059dec67c48968b620e87e3228a7586d0208748e5587893</cites><orcidid>0000-0002-4000-7894 ; 0000-0002-5738-9585 ; 0000-0002-7309-324X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0168827820338174$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33259845$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kupriyanova, Yuliya</creatorcontrib><creatorcontrib>Zaharia, Oana Patricia</creatorcontrib><creatorcontrib>Bobrov, Pavel</creatorcontrib><creatorcontrib>Karusheva, Yanislava</creatorcontrib><creatorcontrib>Burkart, Volker</creatorcontrib><creatorcontrib>Szendroedi, Julia</creatorcontrib><creatorcontrib>Hwang, Jong-Hee</creatorcontrib><creatorcontrib>Roden, Michael</creatorcontrib><creatorcontrib>Roden, M.</creatorcontrib><creatorcontrib>Al-Hasani, H.</creatorcontrib><creatorcontrib>Burkart, V.</creatorcontrib><creatorcontrib>Buyken, A.E.</creatorcontrib><creatorcontrib>Geerling, G.</creatorcontrib><creatorcontrib>Hwang, J.H.</creatorcontrib><creatorcontrib>Herder, C.</creatorcontrib><creatorcontrib>Icks, A.</creatorcontrib><creatorcontrib>Jandeleit-Dahm, K.</creatorcontrib><creatorcontrib>Kahl, S.</creatorcontrib><creatorcontrib>Kotzka, J.</creatorcontrib><creatorcontrib>Kuss, O.</creatorcontrib><creatorcontrib>Lammert, E.</creatorcontrib><creatorcontrib>Trenkamp, S.</creatorcontrib><creatorcontrib>Rathmann, W.</creatorcontrib><creatorcontrib>Szendroedi, J.</creatorcontrib><creatorcontrib>Ziegler, D.</creatorcontrib><creatorcontrib>the GDS group</creatorcontrib><creatorcontrib>GDS group</creatorcontrib><title>Early changes in hepatic energy metabolism and lipid content in recent-onset type 1 and 2 diabetes mellitus</title><title>Journal of hepatology</title><addtitle>J Hepatol</addtitle><description>Non-alcoholic fatty liver disease (NAFLD) is associated with abnormal mitochondrial capacity. While oxidative capacity can be increased in steatosis, hepatic ATP decreases in long-standing diabetes. However, longitudinal studies on diabetes-related NAFLD and its relationship to hepatic energy metabolism are lacking.
This prospective study comprised volunteers with type 1 (T1DM, n = 30) and type 2 (T2DM, n = 37) diabetes. At diagnosis and 5 years later, we used 1H/31P magnetic resonance spectroscopy to measure hepatocellular lipid (HCL), γATP and inorganic phosphate (Pi) concentrations, and to assess adipose tissue volumes. Insulin sensitivity was assessed by hyperinsulinemic-euglycemic clamps.
At diagnosis, individuals with T2DM had higher HCL and adipose tissue volumes, but lower whole-body insulin sensitivity than those with T1DM, despite comparable glycemic control. NAFLD was present in 38% of individuals with T2DM and 7% with T1DM. After 5 years, visceral adipose tissue only increased in individuals with T2DM, while HCL almost doubled in this group (p <0.001), resulting in a 70% prevalence of NAFLD (independent of diabetes treatment). Changes in HCL correlated with adipose tissue volume and insulin resistance (r = 0.50 and r = 0.44, both p <0.05). Pi decreased by 17% and 10% in individuals with T2DM and T1DM (p <0.05), respectively. In T1DM, HCL did not change, whereas γATP decreased by 10% and correlated negatively with glycated hemoglobin (r = -0.56, p <0.05).
The rapid increase in HCL during the early course of T2DM likely results from enlarging adipose tissue volume and insulin resistance in response to impaired hepatic mitochondrial adaptation. The decrease of phosphorus metabolites in T1DM may be due to pharmacological insulin supply.
Previous studies suggested that the impaired function of mitochondria, the power plants of cells, can promote fatty liver and type 2 diabetes mellitus. This study now shows that during the first 5 years of type 2 diabetes the increase in body fat content rapidly leads to a doubling of liver fat content, whereas the energy metabolism of the patients' livers progressively declines. These data suggest that fat tissue mass and liver mitochondria have an important role in the development of fatty liver disease in humans with diabetes.
NCT01055093
[Display omitted]
•Hepatic lipids increase 2-fold in the early course of type 2 diabetes.•Patients with type 1 diabetes do not develop steatosis in first 5 years after diagnosis.•Adipose tissue mass and insulin resistance drive the development of steatosis.•Phosphorus metabolites decline in type 1 diabetes due to low portal insulin supply.</description><subject>Adipose tissue</subject><subject>Adipose Tissue - diagnostic imaging</subject><subject>Adipose Tissue - metabolism</subject><subject>Adipose Tissue - pathology</subject><subject>body composition</subject><subject>Body Composition - physiology</subject><subject>Body fat</subject><subject>Body Fat Distribution</subject><subject>Diabetes</subject><subject>Diabetes mellitus (insulin dependent)</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Diabetes Mellitus, Type 1 - diagnosis</subject><subject>Diabetes Mellitus, Type 1 - metabolism</subject><subject>Diabetes Mellitus, Type 2 - diagnosis</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Diagnosis</subject><subject>Energy metabolism</subject><subject>Energy Metabolism - physiology</subject><subject>Fatty liver</subject><subject>Female</subject><subject>Glycated Hemoglobin A - analysis</subject><subject>Hemoglobin</subject><subject>hepatocellular lipid content</subject><subject>Humans</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Insulin Resistance - physiology</subject><subject>Lipid metabolism</subject><subject>Lipid Metabolism - physiology</subject><subject>Liver - metabolism</subject><subject>Liver - pathology</subject><subject>Liver diseases</subject><subject>Magnetic resonance spectroscopy</subject><subject>Magnetic Resonance Spectroscopy - methods</subject><subject>Male</subject><subject>Metabolism</subject><subject>Metabolites</subject><subject>Middle Aged</subject><subject>Mitochondria</subject><subject>Mitochondria, Liver - physiology</subject><subject>Non-alcoholic Fatty Liver Disease - diagnosis</subject><subject>Non-alcoholic Fatty Liver Disease - metabolism</subject><subject>Phosphorus</subject><subject>phosphorus metabolites</subject><subject>Plant cells</subject><subject>Power plants</subject><subject>Steatosis</subject><issn>0168-8278</issn><issn>1600-0641</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kcFq3DAQhkVJaTZpX6CHIsilF2-lsSTL0EsIaRMI9NKehSzPJnJt2ZXkwL59tdm0hxxyGjF8-hj-n5CPnG054-rLsB0ecNkCg7LgW1azN2TDFWMVU4KfkE2BdKWh0afkLKWBsYK04h05rWuQrRZyQ35f2zjuqXuw4R4T9YEWpc3eUQwY7_d0wmy7efRpojb0dPSL76mbQ8aQD3hEV17VHBJmmvcLUv4EAu297TAX6YTj6POa3pO3Ozsm_PA8z8mvb9c_r26qux_fb68u7yonQOeqhU5yVLxmWsAOulYy2fboVOOEbpXuFDDUDdYA2jZSq74EoBuhUUrd6LY-J5-P3iXOf1ZM2Uw-uXKEDTivyYBQClpQNSvoxQt0mNcYynUGpKylarRoCgVHysU5pYg7s0Q_2bg3nJlDFWYwhyrMoQrDuWFP6k_P6rWbsP__5V_2Bfh6BLBk8egxmuQ8Boe9L6Fm08_-Nf9finSX6A</recordid><startdate>202105</startdate><enddate>202105</enddate><creator>Kupriyanova, Yuliya</creator><creator>Zaharia, Oana Patricia</creator><creator>Bobrov, Pavel</creator><creator>Karusheva, Yanislava</creator><creator>Burkart, Volker</creator><creator>Szendroedi, Julia</creator><creator>Hwang, Jong-Hee</creator><creator>Roden, Michael</creator><creator>Roden, M.</creator><creator>Al-Hasani, H.</creator><creator>Burkart, V.</creator><creator>Buyken, A.E.</creator><creator>Geerling, G.</creator><creator>Hwang, J.H.</creator><creator>Herder, C.</creator><creator>Icks, A.</creator><creator>Jandeleit-Dahm, K.</creator><creator>Kahl, S.</creator><creator>Kotzka, J.</creator><creator>Kuss, O.</creator><creator>Lammert, E.</creator><creator>Trenkamp, S.</creator><creator>Rathmann, W.</creator><creator>Szendroedi, J.</creator><creator>Ziegler, D.</creator><general>Elsevier B.V</general><general>Elsevier Science Ltd</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>H94</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-4000-7894</orcidid><orcidid>https://orcid.org/0000-0002-5738-9585</orcidid><orcidid>https://orcid.org/0000-0002-7309-324X</orcidid></search><sort><creationdate>202105</creationdate><title>Early changes in hepatic energy metabolism and lipid content in recent-onset type 1 and 2 diabetes mellitus</title><author>Kupriyanova, Yuliya ; Zaharia, Oana Patricia ; Bobrov, Pavel ; Karusheva, Yanislava ; Burkart, Volker ; Szendroedi, Julia ; Hwang, Jong-Hee ; Roden, Michael ; Roden, M. ; Al-Hasani, H. ; Burkart, V. ; Buyken, A.E. ; Geerling, G. ; Hwang, J.H. ; Herder, C. ; Icks, A. ; Jandeleit-Dahm, K. ; Kahl, S. ; Kotzka, J. ; Kuss, O. ; Lammert, E. ; Trenkamp, S. ; Rathmann, W. ; Szendroedi, J. ; Ziegler, D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c428t-92b51e6130842f2b95059dec67c48968b620e87e3228a7586d0208748e5587893</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Adipose tissue</topic><topic>Adipose Tissue - 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Academic</collection><jtitle>Journal of hepatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kupriyanova, Yuliya</au><au>Zaharia, Oana Patricia</au><au>Bobrov, Pavel</au><au>Karusheva, Yanislava</au><au>Burkart, Volker</au><au>Szendroedi, Julia</au><au>Hwang, Jong-Hee</au><au>Roden, Michael</au><au>Roden, M.</au><au>Al-Hasani, H.</au><au>Burkart, V.</au><au>Buyken, A.E.</au><au>Geerling, G.</au><au>Hwang, J.H.</au><au>Herder, C.</au><au>Icks, A.</au><au>Jandeleit-Dahm, K.</au><au>Kahl, S.</au><au>Kotzka, J.</au><au>Kuss, O.</au><au>Lammert, E.</au><au>Trenkamp, S.</au><au>Rathmann, W.</au><au>Szendroedi, J.</au><au>Ziegler, D.</au><aucorp>the GDS group</aucorp><aucorp>GDS group</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Early changes in hepatic energy metabolism and lipid content in recent-onset type 1 and 2 diabetes mellitus</atitle><jtitle>Journal of hepatology</jtitle><addtitle>J Hepatol</addtitle><date>2021-05</date><risdate>2021</risdate><volume>74</volume><issue>5</issue><spage>1028</spage><epage>1037</epage><pages>1028-1037</pages><issn>0168-8278</issn><eissn>1600-0641</eissn><abstract>Non-alcoholic fatty liver disease (NAFLD) is associated with abnormal mitochondrial capacity. While oxidative capacity can be increased in steatosis, hepatic ATP decreases in long-standing diabetes. However, longitudinal studies on diabetes-related NAFLD and its relationship to hepatic energy metabolism are lacking.
This prospective study comprised volunteers with type 1 (T1DM, n = 30) and type 2 (T2DM, n = 37) diabetes. At diagnosis and 5 years later, we used 1H/31P magnetic resonance spectroscopy to measure hepatocellular lipid (HCL), γATP and inorganic phosphate (Pi) concentrations, and to assess adipose tissue volumes. Insulin sensitivity was assessed by hyperinsulinemic-euglycemic clamps.
At diagnosis, individuals with T2DM had higher HCL and adipose tissue volumes, but lower whole-body insulin sensitivity than those with T1DM, despite comparable glycemic control. NAFLD was present in 38% of individuals with T2DM and 7% with T1DM. After 5 years, visceral adipose tissue only increased in individuals with T2DM, while HCL almost doubled in this group (p <0.001), resulting in a 70% prevalence of NAFLD (independent of diabetes treatment). Changes in HCL correlated with adipose tissue volume and insulin resistance (r = 0.50 and r = 0.44, both p <0.05). Pi decreased by 17% and 10% in individuals with T2DM and T1DM (p <0.05), respectively. In T1DM, HCL did not change, whereas γATP decreased by 10% and correlated negatively with glycated hemoglobin (r = -0.56, p <0.05).
The rapid increase in HCL during the early course of T2DM likely results from enlarging adipose tissue volume and insulin resistance in response to impaired hepatic mitochondrial adaptation. The decrease of phosphorus metabolites in T1DM may be due to pharmacological insulin supply.
Previous studies suggested that the impaired function of mitochondria, the power plants of cells, can promote fatty liver and type 2 diabetes mellitus. This study now shows that during the first 5 years of type 2 diabetes the increase in body fat content rapidly leads to a doubling of liver fat content, whereas the energy metabolism of the patients' livers progressively declines. These data suggest that fat tissue mass and liver mitochondria have an important role in the development of fatty liver disease in humans with diabetes.
NCT01055093
[Display omitted]
•Hepatic lipids increase 2-fold in the early course of type 2 diabetes.•Patients with type 1 diabetes do not develop steatosis in first 5 years after diagnosis.•Adipose tissue mass and insulin resistance drive the development of steatosis.•Phosphorus metabolites decline in type 1 diabetes due to low portal insulin supply.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>33259845</pmid><doi>10.1016/j.jhep.2020.11.030</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-4000-7894</orcidid><orcidid>https://orcid.org/0000-0002-5738-9585</orcidid><orcidid>https://orcid.org/0000-0002-7309-324X</orcidid><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 0168-8278 |
| ispartof | Journal of hepatology, 2021-05, Vol.74 (5), p.1028-1037 |
| issn | 0168-8278 1600-0641 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2466292630 |
| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Adipose tissue Adipose Tissue - diagnostic imaging Adipose Tissue - metabolism Adipose Tissue - pathology body composition Body Composition - physiology Body fat Body Fat Distribution Diabetes Diabetes mellitus (insulin dependent) Diabetes mellitus (non-insulin dependent) Diabetes Mellitus, Type 1 - diagnosis Diabetes Mellitus, Type 1 - metabolism Diabetes Mellitus, Type 2 - diagnosis Diabetes Mellitus, Type 2 - metabolism Diagnosis Energy metabolism Energy Metabolism - physiology Fatty liver Female Glycated Hemoglobin A - analysis Hemoglobin hepatocellular lipid content Humans Insulin Insulin resistance Insulin Resistance - physiology Lipid metabolism Lipid Metabolism - physiology Liver - metabolism Liver - pathology Liver diseases Magnetic resonance spectroscopy Magnetic Resonance Spectroscopy - methods Male Metabolism Metabolites Middle Aged Mitochondria Mitochondria, Liver - physiology Non-alcoholic Fatty Liver Disease - diagnosis Non-alcoholic Fatty Liver Disease - metabolism Phosphorus phosphorus metabolites Plant cells Power plants Steatosis |
| title | Early changes in hepatic energy metabolism and lipid content in recent-onset type 1 and 2 diabetes mellitus |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-07T20%3A28%3A12IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Early%20changes%20in%20hepatic%20energy%20metabolism%20and%20lipid%20content%20in%20recent-onset%20type%201%20and%202%20diabetes%20mellitus&rft.jtitle=Journal%20of%20hepatology&rft.au=Kupriyanova,%20Yuliya&rft.aucorp=the%20GDS%20group&rft.date=2021-05&rft.volume=74&rft.issue=5&rft.spage=1028&rft.epage=1037&rft.pages=1028-1037&rft.issn=0168-8278&rft.eissn=1600-0641&rft_id=info:doi/10.1016/j.jhep.2020.11.030&rft_dat=%3Cproquest_cross%3E2553567847%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2553567847&rft_id=info:pmid/33259845&rft_els_id=S0168827820338174&rfr_iscdi=true |